Toxicology of PFSAs and PFCAs

There has been considerable interest over the past two decades to investigate the toxicological affects of PFSAs and PFCAs. In particular, the toxicology of PFOS and PFOA has been well studied and reviewed by Lau et al. [22, 23] and Kennedy et al. [24]. 

The pharmacokinetics of PFOS and PFOA have been investigated in animal studies [22-24]. Results indicate that both PFCs are well absorbed following oral exposure, and poorly eliminated. In addition, PFOS and PFOA are very persistent as they are not metabolized and undergo extensive enterohepatic circulation [25,26]. PFSAs and PFCAs are unique among other persistent halogenated organic contaminants as they do not preferentially accumulate in fatty tissues, but instead are predominately distributed in the liver, serum and kidney [22-24]. This may be explained by the fact that PFOS and PFOA bind to proteins, specifically )8-lipoproteins, albumin and liver fatty acid-binding proteins [27, 28]. 

In general, the rate of elimination of PFCAs and PFSAs decreases with increasing length of the perfluoroalkyl tail [23]. Differences in elimination of PFSAs and PFCAs have been 

The chronic toxicity of PFOA has been investigated in a number of animal studies [24]. Typically, tumours are observed in liver cells, Leydig cells (testis) and pancreatic cells [24]. As discussed above, both peroxisome proliferation and inhibition of GJIC can result in tumour growth. An advisory panel to the US Environmental Protection Agency has proposed that PFOA be deemed a rodent carcinogen with relevance to humans [39]. 

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